Separate processes of semantic radicals and phonetic radicals in Chinese character writing : evidence from a Chinese dysgraphic patient

2016-2017 > Academic research: refereed > Refereed conference paperbcwhMetadata onlyPublishe

Expression of heparanase in newborn mouse growth plates

Endochondral ossification is tightly regulated by various heparan sulphate (HS)-binding growth factors, such as fibroblast growth factor 2 and Indian hedgehog. However, HS chains immobilized as substituents on cell surface or matrix proteoglycans are limited in the capacity to present these growth factors efficiently to their corresponding signaling receptors. We hypothesize that heparanase, an endo-E-Dglucuronidase, cleaves HS chains at specific sites to yield mobile HS fragments and avails HS-binding growth factors to their targets. Here we aim to map the expression pattern of heparanase in growth plates of both Hspg2¨3/¨3 , a HS-deficient perlecan mouse mutant, and its wildtype littermates by immunohistochemistry. In both mutant and wildtype animals, heparanase protein was detectable in both the pericellular and extracellular matrix of the resting and proliferative zones but not detectable in the pre-hypertrophic zone. In particular, heparanase is localized in the extracellular matrix of the hypertrophic zone where von Kossa staining of calcium deposits were also found. Our results suggest little involvement of HS moieties of perlecan in the distribution of heparanase and HS-mediated maturation process of the growth plate

Involvement of Calcium/Camodulin-Dependent Kinase II in the Regulation of Vascular Tone in Porcine Coronary Arteries

Poster PresentationConference Theme: Translating Advances in Science into Improvements in Cardiovascular HealthObjectives: Inhibition of calcium/calmodulin-dependent kinase II (CaMKII) has been shown to reduce vascular contraction and relaxation. The present study examined the role of CaMKII in the different signaling pathways involved in the regulation of vascular tone. Methods: Isolated porcine coronary arteries were incubated in organ chamber for the measurement of isometric tension. They were contracted with cumulative additions of contracting agents, potassium chloride and the thromboxane A2 analogue, U46619, or contracted with U46619 (30 nM) followed by cumulative additions of different relaxing agents, in the presence or absence of the CaMKII inhibitor, KN-93. Results: Inhibition of CaMKII by KN-93 (30 μM) significantly inhibited contractions to potassium chloride (10-70 mM) and U46619 (0.1 nM-1 μM) in porcine coronary arteries without endothelium. While endotheliumdependent nitric oxide (NO)-mediated relaxations to bradykinin (0.1 nM- 1 μM) were significantly inhibited by KN-93, endothelium-dependent hyperpolarization (EDH)-mediated relaxations were not affected. On the other hand, KN-93 inhibited endothelium-independent relaxations to levcromakalim (adenosine triphosphate-sensitive potassium channel opener; 0.1 nM-100 μM), but not those to sodium nitroprusside (NO donor; 0.1 nM- 100 μM). Conclusions: Our data suggested that CaMKII in both the endothelium and smooth muscle of porcine coronary arteries plays a role in the regulation of vascular tone. In the smooth muscle, CaMKII contributes to contraction likely via mechanisms downstream of increases in intracellular calcium concentration. It is also involved in the activation of adenosine triphosphatesensitive potassium channels leading to vascular relaxation. In the endothelium, CaMKII appears to play a role in the release of NO, but not the induction of EDH, for relaxation. (This study was supported by the Small Project Funding of the University of Hong Kong Research Grant)

Kaempferol enhances endothelium-independent and dependent relaxation in the porcine coronary artery

The vascular effects of kaempferol were investigated in isolated porcine coronary artery rings. U46619 (9,11-dideoxy-9α, 11α-methanoepoxy prostaglandin F2α, 30 nM) was used to contract porcine coronary arterial rings. Concentration relaxation curve of kaempferol (1 nM - 100 μM) was constructed and kaempferol demonstrated significant relaxation at high concentrations. At low concentration with no significant effect on relaxation, kaempferol (10 μM) enhanced relaxation produced by bradykinin, the calcium ionophore A23187, isoproterenol and sodium nitroprusside in endothelium-intact porcine coronary arteries. In endothelium-disrupt rings, kaempferol (10 μM) also enhanced the relaxation caused by isoproterenol, sodium nitroprusside, levcromakalim and nifedipine. On the other hand, antioxidant agents did not affect bradykinin-induced relaxation or the enhancement effect of kaempferol. In summary, a low concentration of kaempferol (10 μM), devoid of significant vascular effect, has the ability to enhance endothelium-dependent and endothelium-independent relaxations. This action of kaempferol is unrelated to its antioxidant property. © Springer Science+Business Media, Inc. 2006.link_to_subscribed_fulltex

Puerarin, an isoflavonoid derived from Radix puerariae, potentiates endothelium-independent relaxation via the cyclic AMP pathway in porcine coronary artery

Puerarin, an isoflavonoid derived from the Chinese medicinal herb Radix puerariae, has been suggested to be useful in the management of various cardiovascular disorders. The present study examined the effect of acute exposure (30 min) to puerarin on vascular relaxation. Rings from porcine coronary artery of either sex were used. The highest concentration of puerarin (100 μM) produced a small but statistically significant relaxation of U46619-contracted rings. Vascular relaxations were also studied in the presence of lower concentrations of puerarin (0.1, 1 and 10 μM) which had no direct relaxation effect. Puerarin enhanced vasorelaxation to endothelium-independent relaxing agents, sodium nitroprusside and cromakalim. However, puerarin had no effect on vasorelaxation induced by endothelium-dependent relaxing agents, bradykinin and calcium ionophore A23187. The potentiating action of puerarin (10 μM) on sodium nitroprusside-mediated relaxation was not affected by the nitric oxide synthase inhibitor, Nω-nitro-l-arginine methyl ester (l-NAME; 300 μM), or by the disruption of the endothelium with Triton X-100. The effect of puerarin was reversible following a washout period. The potentiating effects were comparable with the 3′-5′-cyclic adenosine monophosphate (cyclic AMP) analogues, 8-bromoadenosine-3′-5′-cyclic monophosphate (8-Br-cyclic AMP; 10 μM) and Sp-isomer [S nomenclature refers to phosphorus] of adenosine-3′, 5′-cyclic monophosphorothioate (Sp-cyclic AMPS; 3 μM), but not the 3′-5′-cyclic guanosine monophosphate (cyclic GMP) analogue, 8-bromoguanosine-3′-5′-cyclic monophosphate (8-Br-cyclic GMP; 3 μM). The cyclic AMP antagonist, Rp-isomer [R nomenclature refers to phosphorus] of 8-bromoadenosine-3′, 5′-cyclic monophosphorothioate (Rp-8-Br-cyclic AMPS; 10 μM), but not cyclic GMP antagonist, Rp-isomer of 8-bromoguanosine-3′, 5′-cyclic monophosphorothioate (Rp-8-Br-cyclic GMPS; 10 μM), reversed the effects of puerarin (10 μM) on the enhancement of vasorelaxation to sodium nitroprusside. Our results demonstrated that puerarin enhanced sodium nitroprusside-induced relaxation, possibly via the cyclic AMP-dependent pathway. © 2006 Elsevier B.V. All rights reserved.link_to_subscribed_fulltex